ArticleOncology letters2022
Auranofin induces urothelial carcinoma cell death via reactive oxygen species production and synergy with cisplatin.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Auranofin Combination Therapy: A New Frontier in Cancer Treatment.Molecules (Basel, Switzerland) · 2026Review
- The gold complex auranofin sensitizes platinum resistant epithelial ovarian cancer cells to cisplatin.Biochemistry and biophysics reports · 2025Article
- A redox-related lncRNA signature in bladder cancer.Scientific reports · 2024Article
- Repurposing auranofin and meclofenamic acid as energy-metabolism inhibitors and anti-cancer drugs.PloS one · 2024Article
- Naturally occurring deamidated triosephosphate isomerase is a promising target for cell-selective therapy in cancer.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Urothelial carcinoma (UC) is one of the most common cancer types of the urinary tract. UC is associated with poor 5-year survival rate, and resistance to cisplatin-based therapy remains a challenge for invasive bladder cancer treatment. Therefore, there is an urgent need to develop new drugs for advanced UC therapy. Auranofin (AF) was developed over 30 years ago for the treatment of rheumatoid arthritis and has been reported to exert an antitumor effect by increasing the level of reactive oxygen species (ROS) in cancer cells. The aim of the present study was to examine the effects of AF on cancer cell proliferation, cell cycle and apoptosis, either alone or in combination with cisplatin. AF induced cell death in two separate cell lines, HT 1376 and BFTC 909, in a concentration- and time-dependent manner by inducing cell cycle arrest. However, the distribution of cells in different phases of the cell cycle differed between the two cell lines, with G
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Registered trials
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